Limits of Exercise Performance
The two main factors that limit skeletal muscle performance in humans are the rate of O2 use by the muscles and the O2 supply to the muscles. However, O2 use by muscle is probably not a critical factor. During exercise, maximal O2 consumption (maximal V˜O2) by a large percentage of the body’s muscle mass is unchanged or increases only slightly when additional muscles are activated. In fact, during exercise of a large muscle mass, as in vigorous bicycling, the addition of bilateral arm exercise without change in the cycling effort produces only a small increase in cardiac output and maximal VO2. However, the additional arm exercise decreases blood flow to the legs. This centrally mediated (baroreceptor reflex) vasoconstriction during maximal cardiac output prevents the fall in blood pressure that would otherwise be caused by metabolically induced vasodilation in the active muscle. If use of O2 by muscles were a significant limiting factor, recruitment of more contracting muscles would entail the use of much more O2 to meet the enhanced O2 requirements.
Limitation of the O2 supply could be caused by inadequate oxygenation of blood in the lungs or limitation of the supply of O2-laden blood to the muscles. Failure by the lungs to oxygenate blood fully can be ruled out because even with the most strenuous exercise at sea level, arterial blood is fully saturated with O2. Therefore, O2 delivery to the active muscles (or blood flow because the arterial blood O2 content is normal) appears to be the limiting factor in muscle performance. This limitation could be caused by the inability to increase cardiac output beyond a critical level. In turn, this inability is caused by a limitation in stroke volume because the heart rate reaches maximal levels before maximal V˜O2 is reached. Hence, the major factor that limits muscle performance is the pumping capacity of the heart.
The response of the cardiovascular system to regular exercise is to increase its capacity to deliver O2 to the active muscles and improve the ability of the muscle to use O2. Maximal
VO2 varies with the level of physical conditioning. Train ing progressively increases maximal VO2, which reaches a plateau at the highest level of conditioning. Highly trained athletes have a lower resting heart rate, a greater stroke volume, and lower peripheral resistance than they had before training or after deconditioning. The low resting heart rate is caused by a higher vagal tone and a lower sympathetic tone. During exercise, the maximal heart rate of a trained individual is the same as that in an untrained person, but it is attained at a higher level of exercise. A trained person also exhibits low vascular resistance in the muscles. If an individual exercises one leg regularly over an extended period and does not exercise the other leg, vascular resistance is lower and maximal V˜O2 is higher in the “trained” leg than in the “untrained” leg.
Physical conditioning is also associated with greater extraction of O2 from the blood (greater arteriovenous O2 difference) by the muscles. With long-term training, capillary density in skeletal muscle increases. Also, an increase in the number of arterioles may account for the decrease in muscle vascular resistance. The number of mitochondria increases, as does the number of oxidative enzymes in mitochondria. In addition, levels of adenosine triphosphatase (ATPase) activity, myoglobin, and enzymes involved in lipid metabolism increase in response to physical conditioning.
Endurancetraining,suchasrunningorswimming,increasesleftventricularvolumewithoutincreasingleftventricularwallthickness.Incontrast,strengthexercises,suchasweightlifting,increaseleftventricularwallthickness(hypertrophy)withlittleeffectonventricularvolume.However,thisincreaseinwallthicknessissmallinrelationtothatobservedinchronichypertension,inwhichafterloadispersistentlyelevatedbecauseofhighperipheralresistance.